Mulkey R M, Zucker R S
Department of Molecular and Cell Biology, University of California, Berkekey 94720.
Nature. 1991 Mar 14;350(6314):153-5. doi: 10.1038/350153a0.
There are two hypotheses to explain how neurons release transmitter. The calcium hypothesis proposes that membrane depolarization is necessary only for opening calcium channels and increasing internal calcium concentration ([Ca2+]i) near membrane transmitter-release sites. These calcium ions trigger a transient release of neurotransmitter. The calcium-voltage hypothesis postulates that voltage induces a conformational change in a membrane protein rendering it sensitive to calcium such that, in the presence of high [Ca2+]i, depolarization directly triggers transmitter release. Here we report that when calcium influx is blocked by cobalt or manganese ions in a calcium-free Ringer, as measured with Fura-2, and [Ca2+]i is elevated by liberation from a caged calcium compound, transmitter release at the crayfish neuromuscular junction is unaffected by presynaptic action potentials. These results support the calcium hypothesis.
关于神经元如何释放递质，有两种假说。钙假说认为，膜去极化仅对打开钙通道和增加靠近膜递质释放位点的细胞内钙浓度（[Ca2+]i）是必要的。这些钙离子触发神经递质的短暂释放。钙-电压假说假定，电压会诱导膜蛋白发生构象变化，使其对钙敏感，从而在高[Ca2+]i存在的情况下，去极化直接触发递质释放。在此我们报告，在用Fura-2测量时，当在无钙林格液中钙内流被钴或锰离子阻断，且[Ca2+]i通过从笼形钙化合物中释放而升高时，小龙虾神经肌肉接头处的递质释放不受突触前动作电位的影响。这些结果支持钙假说。
